Gene Ontology annotation through association of InterPro records with GO terms.
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt.
Gene Ontology annotation based on curation of immunofluorescence data
Quantitative interaction proteomics and genome-wide profiling of epigenetic histone marks and their readers.
CAMP (C13orf8, ZNF828) is a novel regulator of kinetochore-microtubule attachment.
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CHAMP1 is a zinc-finger protein containing WK, SPE, and FPE motifs that localizes to chromosomes and spindle including kinetochores. It undergoes CDK1-dependent phosphorylation during mitosis.
"CAMP is a zinc-finger protein containing three characteristic repeat motifs termed the WK, SPE, and FPE motifs. CAMP localizes to chromosomes and the spindle including kinetochores, and undergoes CDK1-dependent phosphorylation at multiple sites during mitosis"
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CHAMP1-depleted cells showed severe chromosome misalignment associated with poor K-fiber resistance to tension during bi-orientation.
"CAMP-depleted cells showed severe chromosome misalignment, which was associated with the poor resistance of K-fibres to the tension exerted upon establishment of sister kinetochore bi-orientation"
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The FPE region is responsible for spindle and kinetochore localization and is essential for proper chromosome alignment. The C-terminal zinc-finger domains negatively regulate this function.
"the FPE region, which is responsible for spindle and kinetochore localization, is essential for proper chromosome alignment. The C-terminal region containing the zinc-finger domains negatively regulates chromosome alignment"
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CHAMP1 is required for proper kinetochore localization of CENP-E and CENP-F, which are downstream effectors.
"Kinetochore localization of CENP-E and CENP-F was affected by CAMP depletion, and by expressing CAMP mutants that cannot functionally rescue CAMP depletion, placing CENP-E and CENP-F as downstream effectors of CAMP"
A human interactome in three quantitative dimensions organized by stoichiometries and abundances.
DNA Repair Network Analysis Reveals Shieldin as a Key Regulator of NHEJ and PARP Inhibitor Sensitivity.
FAM35A associates with REV7 and modulates DNA damage responses of normal and BRCA1-defective cells.
CHAMP1 binds to REV7/FANCV and promotes homologous recombination repair.
De Novo Mutations in CHAMP1 Cause Intellectual Disability with Severe Speech Impairment.
Deep research summary for CHAMP1
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CHAMP1 binds REV7 via its WKPAKPAPS motif and promotes homologous recombination DNA repair by competing with SHLD3 for REV7 seatbelt binding.
"CHAMP1 is a third REV7 seatbelt-binding partner, and that CHAMP1 binding activates HR repair... The interaction between CHAMP1 and REV7 is mediated by the WKPAKPAPS motif in CHAMP1"
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CHAMP1 knockout reduces HR activity by approximately 60% and sensitizes cells to PARP inhibitors.
"Site-directed mutagenesis creating a CHAMP1-W334A/K335A double mutant (designated CHAMP1-2A) abolished REV7 binding... this mutant failed to rescue the PARP inhibitor sensitivity of CHAMP1 knockout cells"